Darcy B. Adin

Comparison of Canine Cardiac Troponin I Concentrations as Determined by 3 Analyzers

BACKGROUND Recent interest in cardiac biomarkers has led to the validation of several commercial analyzers for cardiac troponin I (cTnI) evaluation in dogs; however, these analyzers have not been standardized. HYPOTHESIS It was hypothesized that canine plasma cTnI concentrations as determined by 3 different analyzers would be similar. ANIMALS Twenty-three dogs with cardiac disease were studied. METHODS Reconstituted purified canine free cTnI was diluted with canine plasma to 8 concentrations (0.01, 0.1, 0.78, 1.56, 3.13, 6.25, 12.5, and 25 ng/mL), for analysis by 3 analyzers, the Biosite Triage Meter, the Dade-Behring Stratus, and the Beckman-Coulter Access AccuTnI. Plasma samples from 23 dogs with cardiac disease were also analyzed for cTnI concentrations on all analyzers. RESULTS Troponin I concentrations in sick dogs were <0.05-5.72 ng/mL (Biosite), 0.02-11.1 ng/mL (Access), and 0.02-9.73 ng/mL (Stratus). Analyzer results were highly correlated with each other (r = 0.97 to 1.0 for purified dilutions, r = 0.61 to 0.89 for samples from dogs); however, the limits of agreement were wide for both purified dilutions and clinical samples. Recovery was highest for the Access (334-1467%) and lowest for the Biosite (38-60%); Stratus 52-233%. Analyzer variability was lowest for the Access (1.2-10.4%) and highest for the Stratus (4.8-33.6%); Biosite 2.8-16.5%. CONCLUSIONS AND CLINICAL IMPORTANCE Results from this study suggest that although canine cTnI values obtained from the Biosite, Stratus, and Access analyzers are closely correlated, they cannot be directly compared with each other. In the absence of a gold standard none of the analyzers can be considered more correct than the others.

Physiologic valve regurgitation in normal cats

OBJECTIVE The purpose of this study was to evaluate echocardiograms from normal cats for the presence of physiologic valve regurgitation (PVR). BACKGROUND PVR occurs commonly in normal dogs, however, the percentage of normal cats with PVR has not been previously reported. ANIMALS, MATERIALS AND METHODS Echocardiograms were retrospectively and prospectively evaluated from clinically normal cats without echocardiographic evidence of cardiac disease. PVR was diagnosed if the valve was structurally normal and regurgitant color flow was subjectively trivial. The color jet area was expressed as a percentage of the chamber area. Results are expressed as mean+/-SD. RESULTS Retrospective study: The 46 cats were 2.1+/-1.5 years (range 0.3-7 years) and were purebred. Four cats (9%) had physiologic mitral regurgitation (PMR) (area of 4%). One cat (2%) had physiologic pulmonary regurgitation (PPR). Twenty-seven cats (57%) had physiologic tricuspid regurgitation (PTR) (area of 6+/-3% to 11+/-8% depending on view). Prospective study: The 58 cats were 4.9+/-2.8 years (range 1-12 years), weighed 5.2+/-1.2kg and were of various breeds. Three cats (5%) had PMR (area of 10+/-2%). One cat (2%) had PPR. Forty-one cats (71%) had PTR (area of 9+/-5% to 11+/-6% depending on view). Retrospective and prospective data were pooled (104 cats) and 7 cats (7%) had PMR, 2 cats (2%) had PPR and 68 cats (65%) had PTR. CONCLUSIONS PTR is common in normal cats and the average regurgitant jet area is small compared to the chamber area.

Successful closure of left-to-right patent ductus arteriosus in three dogs with concurrent pulmonary hypertension.

Closure of reversed patent ductus arteriosus (PDA) is generally accepted to be contraindicated due to case based evidence of worsened outcomes, but little is known about closure of left-to-right PDA with concurrent pulmonary hypertension (PH). This report describes three dogs presenting with varying severity of PH and clinical signs, all with documented left-to-right PDA. The PDA was closed in each case; either by surgical ligation or transarterial device occlusion, and follow up was available for a minimum of 8 months. Every case had a successful outcome with improvement or resolution of PH and associated clinical signs.

Effect of routine cardiovascular catheterization on cardiac troponin I concentration in dogs

OBJECTIVE To determine changes in cardiac troponin I concentration (cTnI) associated with cardiovascular catheterization in dogs. ANIMALS, MATERIALS AND METHODS cTnI was measured after transarterial coil embolization of patent ductus arteriosus (PDA), balloon valvuloplasty (BV), and pacemaker implantation (PACE). Dogs undergoing ovariohysterectomy (OHE) were used as a control, with 15 animals in each group. Blood for the cTnI assay was collected at baseline (T0), at 5h (T5), 24h (T24) and 10 days (T240) post-procedure. The effects of age, duration and difficulty of the procedure were evaluated. RESULTS There was no difference in cTnI concentration at T0 for any of the groups. There was a significant increase in cTnI concentration for BV and PACE, but not PDA at T5 and T24. PACE at T24 and T240 also had higher cTnI than control. Dogs with longer procedure times had significantly higher concentration of cTnI. There was no correlation between the difficulty of the procedure or peri-procedure complications and cTnI. CONCLUSION cTnI increased during some cardiovascular catheterization procedures, but returned to normal values at 24-240 h. Patients undergoing long catheterization procedures have increased risk for myocardial injury, but this was not related to short-term prognosis.

Effect of atenolol on heart rate, arrhythmias, blood pressure, and dynamic left ventricular outflow tract obstruction in cats with subclinical hypertrophic cardiomyopathy.

OBJECTIVE To investigate the negative chronotropic, antiarrhythmic, and obstruction-relieving effects of atenolol in cats with subclinical hypertrophic cardiomyopathy (HCM). ANIMALS Seventeen cats with HCM. METHODS Results for echocardiography, electrocardiography, Doppler blood pressure, and 24 h Holter monitoring were compared in cats before and 2-4 weeks after atenolol therapy (6.25-12.5 mg PO q 12 h). RESULTS The left ventricular outflow tract maximum velocity (LVOT Vmax) decreased after atenolol administration (mean Vmax pre-treatment 3.3 m/s ± 1.8 m/s; post-treatment 1.6 m/s ± 1.0 m/s, p < 0.0001). Heart rate (HR) decreased after atenolol for all HR modalities. The total number of ventricular origin complexes (TotVent) and ventricular premature complexes (VPCs) decreased after atenolol. The VPCs decreased from a geometric mean of 61 complexes/24 h (range, 11-620 complexes/24 h) to 15 complexes/24 h (range, 1-1625 complexes/24 h) (p < 0.0001). Murmur grade decreased after atenolol from a median grade of 3/6 to 2/6 (p < 0.0001). The systolic blood pressure did not change (mean pre-treatment 130 mmHg ± 16 mmHg, mean post-treatment 123 mmHg ± 20 mmHg, p = 0.2). CONCLUSION Atenolol decreases HR, murmur grade, and LVOT obstruction, and to a lesser degree, frequency of ventricular ectopy, in cats with subclinical HCM. Further studies are needed to determine if sudden cardiac death or long-term outcome is influenced by atenolol administration.

Angiotensin-converting enzyme activity in Cavalier King Charles Spaniels with an ACE gene polymorphism and myxomatous mitral valve disease

Objectives Myxomatous mitral valve disease (MMVD) is the most common heart disease in the dog. It is particularly common in the Cavalier King Charles Spaniel (CKCS) breed and affected dogs are frequently managed with angiotensin-converting enzyme inhibitors (ACE-I). We have previously identified a canine ACE gene polymorphism associated with a decrease in angiotensin-converting enzyme (ACE) activity. The aim of this study was to evaluate for the prevalence of the ACE polymorphism in CKCS with mitral valve disease and to determine whether the presence of the polymorphism is associated with alterations in ACE activity at different stages of cardiac disease. Methods Seventy-three dogs with a diagnosis of mitral valve disease were evaluated and a blood sample was drawn for ACE polymorphism genotyping and ACE activity measurement. Results Forty-three dogs were homozygous for the ACE polymorphism; five were heterozygous and 25 were homozygous wild type. The mean age and the median severity of disease were not different for dogs with the polymorphism and dogs with the wild-type sequence. The median baseline ACE activity was significantly lower for the ACE polymorphism (27.0 U/l) than the wild-type sequence dogs (31.0 U/l) (P=0.02). Dogs with more severe disease and the ACE polymorphism had significantly lower levels of ACE activity than dogs with the wild-type sequence (P=0.03). Conclusion The CKCS appears to have a high prevalence of the ACE variant. Dogs with the ACE variant had lower levels of ACE activity even in more advanced mitral valve disease than dogs without the variant. The clinical significance of this finding and its impact on the need for ACE-I in dogs with the polymorphism and heart disease deserves further study.